Luminal A (ER+; PR+; HER2−) BC subtype progression is supported by deregulated ER activation via the binding of its ligand, estrogen, or by estrogen-independent receptor activation by Tyrosine Kinase Receptors (RTKs), including Epidermal Growth Factor (EGFR), HER2, Insulin-like Growth Factor 1 (IGF-1R), PI3K/Akt/mTOR, or MAPK1. This evidence concerns the gene MAPK1 and breast cancer.